Post-transfusion purpura (PTP) with severe thrombocytopenia occurred eight days after transfusion in a 28-year-old woman and responded to treatment with prednisone and plasma exchange. In contrast to nearly all previously studied cases of PTP, the patient's platelets were PlA1-positive and anti-PlA1 antibody could not be detected in serum obtained during the thrombocytopenic episode. Her serum was found to contain an antibody specific for a recently described platelet-specific alloantigen, Baka, in addition to multiple HLA-specific antibodies. The patient's platelets, typed following recovery, were Baka-negative. These findings indicate that post-transfusion purpura can occur in association with alloimmunization to platelet-specific antigens other than PlA1. In performing the serologic studies, a close relationship and possible identity between Baka and another recently reported platelet antigen, Leka, was observed. A method for analyzing mixtures of cytotoxic platelet-reactive antibodies without separating the individual antibodies is described.

The effect of platelet type-specific transfusion in posttranfusion purpura is reported. Seven days after receiving 4 units of whole blood during total hip replacement a 69-year-old woman developed fulminant thrombocytopenic purpura. Her undiluted serum inhibited the clot retraction of PlAl-positive but not PlAl-negative blood. Anti-PlAl titer of her serum, determined by 51Cr platelet lysis technique, was 1:64. The serum had no lytic activity against platelet-rich plasma from two PlAl-negative donors. No anti-HLA antibody was detectable in the serum by lymphocytotoxicity technique, and serum obtained prior to transfusions had no platelet lytic activity. Four units of PlAl-negative platelet concentrate were administered, the first instance in which this treatment has been used. No rise in platelet count ensued, and the patient succumbed to purpura. Exchange transfusion or plasmapheresis remain the treatments of choice.

In four groups of subjects free of thyroid disease, the following determinations were made: serum concentrations of thyroxine (T4), triiodothyronine (T3), reverse T3(rT3) and diiodothyronine (T2), and calculated indices of free thyroxine (FT4) and free triiodothyronine (FT3). Group A comprised healthy subjects aged 16-64; Group B, 24 healthy elderly subjects aged 68-95; Group C, 23 elderly patients with mild well-controlled chronic illnesses, aged 70-85; Group D, 40 nursing home residents aged 66-100. Serum T4 and T2 concentrations and the FT4 index were not affected by age; the rT3 concentration was slightly but significantly elevated only in Group D patients. Serum T3 concentration was significantly lower in all groups of elderly subjects and decreased FT3 index measurements were detected after age 75. It was concluded that old age, without complicating illness, is accompanied only by a decrease in the serum level of T3 and the FT3 index; values for other iodothyronines are unchanged. Clinicians should consider the age-related changes in T3 and FT3 values when interpreting thyroid function tests.

Several tests of thyroid function were performed in 35 hyperthyroid patients over the age of 65 (elderly). The results were compared to those of similar tests in 48 hyperthyroid patients under the age of 65 (young). Total serum thyroxine (T4) was within the normal range in 14 percent of the elderly and 11 percent of the young hyperthyroid patients. The free thyroxine index (FTI) was within the normal range in 11 percent of both groups. The triiodothyronine uptake (T3U) proved to be a poor test in both groups. Although elevation of the triiodothyronine (T3) level allowed a diagnosis of "T3-toxicosis" in 2 elderly and 3 young hyperthyroid patients, the T3 level was normal in 34 percent of the elderly and 13 percent of the young subjects. Correction of the T3 range for age reduced the number of normal T3 values to 12.5 percent in the elderly hyperthyroid patients. The 24-hour uptake of radioactive iodine was normal in 12 percent of the young hyperthyroid patients, 27 percent of the elderly patients with Graves' disease, and 70 percent of the elderly patients with toxic nodular goiter, despite recent readjustment of the normal range for the test. It is concluded that the diagnosis of hyperthyroidism in the elderly may be difficult and that no single test can be relied upon to exclude the diagnosis.

We examined the mechanism by which hypertriglyceridemia interferes with the Roche Diagnostics "Amylochrome" procedure for measurement of amylase in lactescent samples with normal and above-normal amylase activity. The serum blank recommended in the Amylochrome protocol to compensate for lactescence remains inappropriately turbid, compared with the test, and is partly responsible for the underestimation of amylase activity. Other major interference is seen when lipoprotein in hyperlipemic samples with above-normal amylase activity reacts with the soluble oligosaccharide-triazinyl dye product of the Amylochrome assay to form a flocculent blue precipitate. The formation of this precipitate in the test, and its removal, diminish lactescence due to lipemia, an effect that cannot be matched by any manipulation of a serum blank procedure. Oligosaccharide-dye product is removed as a component of the precipitate.

SummaryPlatelet acetylcholinesterase (AChE) activity was measured in gel-filtered platelet preparations. Three different anticholinesteratic agents (eserine, neostigmine, and diiso- propylphosphorofluoridate) at final concentrations of 10 μM caused complete inhibition of AChE activity after 30 min incubation at room temperature with either platelet-rich plasma or gel-filtered platelets. Complete inhibition of platelet AChE had no effect on platelet aggregation, factor-3 availability, and plasma clot retraction. We conclude that platelet membrane AChE activity is not required for normal platelet function as measured by these in vitro parameters.

No abstract